PMID- 18845325
OWN - NLM
STAT- MEDLINE
DCOM- 20081210
LR  - 20141120
IS  - 1097-6825 (Electronic)
IS  - 0091-6749 (Linking)
VI  - 122
IP  - 5
DP  - 2008 Nov
TI  - Aberrant function of peripheral blood myeloid and plasmacytoid dendritic cells in 
      atopic dermatitis patients.
PG  - 969-976.e5
LID - 10.1016/j.jaci.2008.08.028 [doi]
AB  - BACKGROUND: Dendritic cells (DCs) can act both as innate cells in host defense 
      and as antigen-presenting cells for naive T cells in adaptive immunity. These 
      functions, among others, are determined by the level of production of particular 
      cytokines. Atopic dermatitis (AD) is a chronic inflammatory skin disorder 
      characterized by an initial phase predominated by T(H)2 cytokines that switches 
      into a second, more chronic T(H)1-dominated eczematous phase. OBJECTIVE: To 
      assess to what extent the AD phenotype is associated with an aberrant phenotype 
      and function of DCs. METHODS: Classic CD1c(+)/blood DC antigen (BDCA)-1(+) 
      myeloid (m) DCs and CD304(+)/BDCA4(+) plasmacytoid (p) DCs, the natural 
      IFN-producing cells, were isolated from peripheral blood of patients with AD and 
      healthy controls and analyzed for their phenotype and function. RESULTS: Purified 
      CD1c(+)/BDCA1(+) mDCs from patients with AD showed a selective and dramatic 
      reduction of IL-12p70 and TNF-alpha release. IL-12p70 reduction was attributed to 
      a defective expression of both IL-12p35 and IL-12p40 subunits. Accordingly, 
      mature CD1c(+)/BDCA1(+) mDCs from patients with AD induced considerably less 
      IFN-gamma-producing and more IL-4-producing T(H) cells compared with mDCs from 
      healthy controls. In addition, CD304(+)/BDCA4(+) pDCs from patients with AD 
      produced significantly lower levels of IFN-alpha compared with healthy controls. 
      CONCLUSION: Myeloid DCs and pDCs from patients with AD show defective IL-12, 
      TNF-alpha, and IFN-alpha production, which may contribute to increased 
      susceptibility to infection and to the maintenance of the T(H)2 cell-mediated 
      allergic state in patients with AD.
FAU - Lebre, M Cristina
AU  - Lebre MC
AD  - Department of Cell Biology and Histology, Academic Medical Centre, University of 
      Amsterdam, Amsterdam, The Netherlands.
FAU - van Capel, Toni M M
AU  - van Capel TM
FAU - Bos, Jan D
AU  - Bos JD
FAU - Knol, Edward F
AU  - Knol EF
FAU - Kapsenberg, Martien L
AU  - Kapsenberg ML
FAU - de Jong, Esther C
AU  - de Jong EC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081009
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Antigens, CD1)
RN  - 0 (Antigens, Surface)
RN  - 0 (CD1C protein, human)
RN  - 0 (Cytokines)
RN  - 0 (Glycoproteins)
SB  - IM
MH  - Adult
MH  - Antigens, CD1/genetics/immunology
MH  - Antigens, Surface/genetics/immunology
MH  - Cytokines/immunology
MH  - Dendritic Cells/*immunology
MH  - Dermatitis, Atopic/genetics/*immunology
MH  - Female
MH  - Glycoproteins/genetics/immunology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myeloid Cells/*immunology
MH  - Phenotype
MH  - Young Adult
EDAT- 2008/10/11 09:00
MHDA- 2008/12/17 09:00
CRDT- 2008/10/11 09:00
PHST- 2008/02/05 00:00 [received]
PHST- 2008/07/08 00:00 [revised]
PHST- 2008/08/04 00:00 [accepted]
PHST- 2008/10/11 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/10/11 09:00 [entrez]
AID - S0091-6749(08)01553-4 [pii]
AID - 10.1016/j.jaci.2008.08.028 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2008 Nov;122(5):969-976.e5. doi: 
      10.1016/j.jaci.2008.08.028. Epub 2008 Oct 9.